It has been suggested that chronic interstitial lung disease usually exhibits a component of inflammation and not infrequently, evidence of immunological involvement. The objectives of this SCOR are to examine the contribution of inflammation and the immune system, and in particular the involvement of immune complexes in idiopathic (and other) interstitial pneumonitides. Studies of the mechanisms of pulmonary inflammation will include examination of: a) Initiating events, especially those mediated by biologically active fragments of the complement system; b) controlling and modulating processes (immunologic and non-immunologic) which would normally serve to limit the progression of the inflammatory reaction; c) reparative re-epithelialization mediated by type II pneumocytes, defects in which may significantly contribute to later fibrosis. The canine model of bleomycin-induced inflammation and fibrosis will be used to examine the hypothesis that acute inflammation (e.g. neutrophil infiltration) represents a determinant of disease progression, that these cellular (inflammatory) stages of the model can be detected non-invasively, and that treatment at this stage will be more effective. Finally, these same questions of mechanism and significance of acute inflammatory processes and immune complexes will be asked of patients with interstitial lung disease.